title: [Effect of hydrogen sulfide donor NaHs on the functional state of the respiratory chain of the rat heart mitochondria].
abstract: In experiments on mitochondria isolated from the heart tissue of adult rats we studied the effects of a donor of hydrogen sulfide, NaHS, on the respiratory chain of the organelles. We found that NaHS (10(-9)-10(-6) mol/l) caused a dose-dependent decrease in the rate of oxygen consumption in the presence of succinate and ADP (state 3 to Chance), and in the absence of ADP (state 4). The decrease in the rate of oxygen consumption in a concentration NaHS 10(-9) mol/l and 10(-8) mol/l associated with an increased conjugation of oxidation and phosphorylation, as evidenced by the increase in the respiratory control, the efficiency of oxidative phosphorylation (ADP/O) is not changed. Our studies suggest a protective effect of hydrogen sulfide donor on the functional state of the mitochondria. To elucidate of other the mechanisms of the protective action H2S we also investigated the effect of hydrogen sulfide donor on the mitochondrial swelling. It was found that NaHS in the range of concentration 10(-12) - 10(-4) mol/l influences the level of mitochondria swelling of the rats heart in the dose-dependent manner. It was also shown that when the concentration of Ca2+ 1 nmol/mg protein in the medium, under the action of hydrogen sulfide in the donor concentration range 10(-12) - 10(-8) mol/l, there was a moderate swelling of rats heart mitochondria. Under the action of NaHS at a concentration of 10(-9) mol/l it was observed swelling of the mitochondria, the maximum change in the level of which was 11%. Inhibitor of mitochondrial ATP-sensitive K+ channels (K(ATP) channels) 5-hydroxydecanoate (10(-4) mol/l) partially reduced the mitochondrial swelling in the presence of NaHS (10(-9) mol/l), which may indicate the activation of K(ATP) channels. Our studies point for possible involvement of mitochondrial K(ATP) channels in implementation of the mechanisms of H2S.
authors.forename: O M
authors.initials: OM
authors.lastname: Semenykhina
authors.forename: N A
authors.initials: NA
authors.lastname: Strutyns'ka
authors.forename: A Iu
authors.initials: AIu
authors.lastname: Bud'ko
authors.forename: H L
authors.initials: HL
authors.lastname: Vavilova
authors.forename: V F
authors.initials: VF
authors.lastname: Sahach
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D004305:Dose-Response Relationship, Drug; D004579:Electron Transport / Q000187:drug effects; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology*; D008933:Mitochondrial Swelling / Q000187:drug effects; D010085:Oxidative Phosphorylation / Q000187:drug effects; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013386:Succinates / Q000494:pharmacology; D013440:Sulfides / Q000494:pharmacology
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D013386:Succinates; D013440:Sulfides; C117780:mitochondrial K(ATP) channel; D000244:Adenosine Diphosphate; C025451:sodium bisulfide; D006862:Hydrogen Sulfide